Periodontoolasia, the general term for degenerative and destructive diseases of the periodontium, is a pervasive problem in the human mouth, especially in those persons 60 years of age and older. The pathogenesis is complex (see generally Lindhe, J., Textbook of Clinical Periodontology (Munksgaard/Saunders 1985)) and may take years to manifest into more advanced stages of disease. Multiple factors combine, the most important being bacteria, which initiate plaque eventuating in gingivitis, the inflammation of the gingiva or gums. Left untreated, epi- and subgingival colonies of bacteria or plaque continue to expand, causing the condition of the gingiva to worsen from acute to chronic gingivitis. There is currently no method to stop the formation and existence of plaque other than mechanical removal by, for example, scraping with dental tools.
At the chronic stage of infection and inflammation, pockets dissect between the teeth and gingiva. Macrophages accumulate and begin to secrete prostoglandins, interleukins and collagenase, which cause inflammation and destruction of the surrounding tissues. As the lesions deepen, the gingival tissues become less able to adhere to the tooth surface and become thinner, more friable and sometimes ulcerated. A deepened gingival sulcus or pocket is formed (an overt indication used to measure the severity of periodontal disease), allowing for greater subgingival bacterial infection. This deepening of the sulcus is clinically seen as gum recession.
The bacteria typically present in the early and late stages of disease and especially in the interstitial pockets of fluid are collagenase producing. Collagenase is an enzyme that destroys the protein complex, collagen. Collagen, the protein forming collagenous fibers of the skin, tendon, ligaments, bone and all other connective tissue, is the fundamental component of the network holding together the individual tooth, the periodontium and the bone surrounding and anchoring the tooth to the bone. The collagenase produced by bacteria destroys the collagen fibers which form the periodontal ligament; the tooth loosens and falls out.
The periodontal ligament attaches the tooth to the dental alveolus. The periodontal ligament is also called the periodontal membrane, but neither term adequately describes its structure or function. In addition to providing support for the tooth, the periodontal ligament provides for nutrition of adjacent structures, proprioception and tooth eruption in the juvenile mouth. Degeneration or destruction of the periodontal ligament results in loose teeth, difficultly in mastication, general soreness and pain. As the periodontal disease progresses, alveolar bone resorption occurs, leading to tooth loss.
In many persons, generally over 60 years of age, bacterially initiated periodontoclasia may be exacerbated or periodontoclasia may be independently induced by the general deterioration of the periodontium, generally called senile atrophy, senescence or regressive change. Atrophy of tissues is a characteristic and unavoidable consequence of the aging process. In senile atrophy, skin thins and, particularly in the mucosal and periodontal tissues of the mouth, older persons experience a decrease in cardiovascular flow; mucous glands involute and glandular activity generally reduces; proliferitive or cell renewal activity slows down; blood vessels decrease in number; and the periodontium tends to become thinner, more friable, and more vulnerable to infection; hence, increased prevalence with age.
Methods of the prior art have attempted to cure periodontoclasia by using bacteriostatics, such as chlorhexidine and tetracycline. Such bacteriostatic treatments, however, do nothing to alleviate the inflammatory responses accompanying diseases of the periodontium. Chlorhexidine treatment, for example, is generally unsuitable for practical use in humans because chlorhexidine stains the teeth black. In addition, bacteriostatics have limited effectiveness, are generally not appropriately administered for long periods of time (i.e. for chronic conditions) and are best administered only at the acute stage of the disease. Because periodontal disease and regressive changes in the periodontium may occur progressively over years, bacteriostatics and do not provide adequate treatment for periodontoclasia.
Other prior methods have attempted to alleviate the inflammatory responses of the periodontium and surrounding interstices. Ibuprofen, produced by Upjohn and other manufacturers, is one example of a medication designed to alleviate inflammation, mainly in arthritis. Ibuprofen and other anti-inflammatory treatments, such as Motrin, Advil and steroids (e.g., cortisone) administration, are known to potentiate infection. However, ibuprofen barely moderates gingivitis, and results are inconsistent. Moreover, high doses, typically 1,600 to 2,400 milligrams, are required for periodontal anti-inflammatory response. Ibuprofen may be generally used at the acute stage for flare-ups, but not the chronic stage. Many patients are unsuitable candidates for ibuprofen administration because of gastric bleeding and ulceration.
Further, the prior uses of anti-inflammatories and bacteriostatics are ineffective against senile atrophy and do nothing to repair or reverse periodontoclasia in general. Antibiotics, and anti-inflammatories are generally inadequate for use as preventative therapy against degenerative and destructive disease.
Russian Patent No. 950,387, issued to Sklyar, et al., discloses the use of Vitamin A (retinol) and Vitamin E to treat tooth decay and inflammation of the mucous membranes of the oral cavity. My efforts to use retinol (0.5% by weight concentration) demonstrated that Vitamin A has no effect on periodontoclasia. It is believed that retinol is metabolized to retinal quickly when topically applied in the oral cavity and is rendered ineffective in treating periodontoclasia.
Mixtures of Vitamins A, E and K were claimed to improve the status of periodontium in Khmelevskii, et al., "Vliianie Vitaminov A, E, K na Pokazateli Glutationovoi Antiperekisnoi Sistemy v Tkaniakh Desny pri Parodontoze," Vopr Pitan, 4:54 (1985). These vitamins were discussed as useful antioxidants. Retinol, however, is not believed to be effective in treating periodontoclasia, as discussed above.
In view of the serious deficiencies of the prior art, it would be desirable to have methods of retarding and reversing periodontoclasia and gingivitis generally and particularly periodontoclasia and gingivitis due to senile atrophy that is safe, corrective, and usable in preventative or maintenance therapy.